Evidence map›Paper›PMID 35365453›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2022

[Hyperactivation of PI3K/AKT/mTOR signal pathway impairs TNF-α-induced autophagy in mesenchymal stem cells from patients with ankylosing spondylitis].

Z Liu, S Min, X Lu, S Cen, Z Chen, T Wang, J Li, W Zeng, S Qiu

Open access · greenAbstract read
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Z LiuDepartment of Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
S MinDepartment of Orthopedics, Shenzhen Hospital, Peking University, Shenzhen 518034, China.
X LuDepartment of Dermatology, Fourth Affiliated Hospital of Guangzhou Medical University, Guangzhou 510316, China.
S CenDepartment of Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
Z ChenDepartment of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat- sen University, Guangzhou 510120, China.
T WangDepartment of Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
J LiDepartment of Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
W ZengDepartment of Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
S QiuDepartment of Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
Southern Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the changes in autophagy of mesenchymal stem cells (MSCs) from patients with ankylosing spondylitis and explore the mechanism for decreased autophagy in ASMSCs.

methodsMSCs collected from 14 patients with AS (ASMSCs) and from 15 healthy donors (HDMSCs) were cultured in the absence or presence of 25 ng/mL TNF-α for 6 h. Autophagy of the cells was determined by immunofluorescence staining of GFP-LC3B, and the results were confirmed by detecting the protein expressions of autophagy markers LC3 II/LC3 I and P62. The mRNA expressions of the related genes were detected using qRT-PCR, and the protein expressions of the autophagy markers and signaling pathway-related molecules were determined with Western blotting. TG100713 was used to block the PI3K/AKT/mTOR signal pathway, and its effect on autophagy of ASMSCs was evaluated.

resultsASMSCs showed significantly weaker GFP-LC3B puncta staining and lower protein expression levels of LC3 II/LC3 I but higher levels of P62 protein (

conclusionIn patients with AS, hyperactivation of the PI3K/AKT/mTOR signaling pathway results in decreased autophagy of the MSCs and potentially contributes to chronic inflammation.

Indexed as

Mesenchymal Stem CellsSpondylitis, AnkylosingAutophagyHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTumor Necrosis Factor-alphaMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTumor Necrosis Factor-alphaankylosing spondylitisautophagymesenchymal stem cellstumor necrosis factor-α

Identifiers

PMID35365453
PMCPMC8983359
OpenAlexW4224142365

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.